This document summarizes hemodynamic disorders and edema. It defines edema as abnormal excessive accumulation of fluid in tissues and serous cavities. Edema can be localized or generalized depending on its cause and distribution. The key mechanisms of edema formation are increased hydrostatic pressure, decreased plasma oncotic pressure, lymphatic obstruction, and sodium and water retention. Specific types of edema like pulmonary edema, cerebral edema, hepatic edema, and renal edema are also discussed. The document compares the characteristics of transudate and exudate fluids and provides diagrams to illustrate the pathogenesis of different types of edema.

1. HEMODYNAMIC
DISORDERS(OEDEMA)-
PART-I
Dr. Babai Halder
Asst. Professor(Pathology)

2. Overview• HEMODYNAMIC deals with the circulation of the blood/ the
forces or mechanisms involved in circulation.
• Hemodynamic Disorders-
• Edema (increased fluid in the ECF)
• Hyperemia (INCREASED flow)
• Congestion (INCREASED backup)
• Hemorrhage (extravasation)
• Thromboembolic Disease-
• Thrombosis (clotting blood)
• Embolism (downstream travel of a clot)
• Infarction (death of tissues w/o blood or ischemia)
• Shock-
• Shock (circulatory failure/collapse)

3. HOMEOSTASIS
• The mechanism by which the constancy of
the internal environment is maintained and
ensured is called the homeostasis.
• Claude Bernarde (1949) – internal
environment or milieu interieur
• Internal envt – water and electrolytes

4. FLUID COMPARTMENTS

5. • STERLING’S FORCES
• HYDROSTATIC PRESSURE - capillary blood pressure -
drives fluid through the capillary wall into the interstitial
space.
• COLLOID OSMOTIC PRESSURE - exerted by proteins
present in the ECF - tends to draw fluid into the vessels.

7. NORMAL FLUID EXCHANGES

8. OEDEMA- DEFINITION
The greek word ‘oidema’ means swelling.
Edema is defined as abnormal and excessive
accumulation of “free fluid” in the interstitial tissue
spaces and serous cavities.
-Edema occurs in both extracellular and intracellular
fluid compartment (mainly in the ECF)
-Depending on its cause and mechanism,edema may
be localized or have a generalized distribution
-Depending on the composition of fluid: transudate &
exudate oedema

9.  PATHOPHYSIOLOGICAL CATEGORIES OF
EDEMA
A) ↑ed hydroststic pressure :
• Impaired venous return :
CHF
Constrictive pericatditis
Ascites (liver cirrhosis)
Venous obstruction or compression(thrombosis,
external pressure etc.)
•Arteriolar dilation :
Heat
Neurohumoral dysregulation
B) ↓ed plasma osmotic
pressure( hypoproteinemia):

10. C)Lymphatic obstruction
•Inflammatory
•Neoplastic
•Postsurgical
•Postirradiation
D)Sodium retention
•Excessive salt intake with renal insufficiency
•↑ed tubular reabsorption of sodium
•Renal hypoperfusion
•↑ed renin-angiotensin-aldosterone secretion
E)Inflammation
•Acute inflammation
•Chronic inflammation

11. PATHOGENESIS:-
• The following mechanisms may be operating singly or in
combination to produce oedema:
1. Decreased plasma oncotic pressure
2. Increased capillary hydrostatic pressure
3. Lymphatic obstruction
4. Tissue factors (increased oncotic pressure of interstitial
fluid, and decreased tissue tension)
5. Increased capillary permeability
6. Sodium and water retention.

12. Diagrammatic representation of pathogenesis of oedema (OP = oncotic pressure; HP = hydrostatic pressure). A,
Normal pressure gradients and fluid exchanges between plasma, interstitial space and lymphatics. B, Mechanism of
oedema by decreased plasma oncotic pressure and hypoproteinaemia. C, Mechanism of oedema by increased
hydrostatic pressure in the capillary. D, Mechanism of lymphoedema. E, Mechanism by tissue factors (increased
oncotic pressure of interstitial fluid and lowered tissue tension). F, Mechanism of oedema by increased capillary
permeability.

13. 1) STERLING FORCES :-
↑ed hydrostatic pressure
and ↓ed colloidal oncotic pressure of vascular
system
movement of fluid from the vascular to
the extravascular space
•↑ed hydrostatic pressure – seen in obstruction in venous
drainage. It may be generalized,e.g., CHF.
•↓ed colloidal osmotic pressure of plasma– seen in cases
that induce hypoproteinemia,e.g., nephrotic syndrome,
malnutrition.

14. 2)LYMPHATIC OBSTRUCTION:-
impaired lymphatic drainage
impaired fluid return from interstitial
space into vascular compartment
lymphedema
It can result from
inflammatory,neoplastic,postsurgical,
post-irradiation, obstruction of lymphatics ,e.g.,
filariasis (elephantiasis), carcinoma of the
breast(peau d’orange)

15. 3) SODIUM AND WATER RETENTION:-
↓ed effective arterial volume(as seen in heart
failure, nephrotic syndrome,cirrhosis etc.)
renal efferent arteriolar constriction
and an elevation of filtration fraction
↓ed hydrostatic and ↑ed colloidal osmotic
pressure of peritubular capillaries
↑ed tubular reabsorption (proximal tubule
and ascending limb of loop of Henle)Na + H2O
↑ ed plasma volume
edema

16. 4) RENIN—ANGIOTENSIN—ALDOSTERONE (RAA)
SYSTEM
In conditions associated with diminished
renal blood flow there is release of renin by the
renal juxtaglomerular cell.

17. Renin
Angiotensinogen Angiotensin I(decapeptide)
(an α2 globulin synthesized by liver)
Angiotensin II(octapeptide)
(vasoconstriction and Na+ (angio-IIacts on zona
and water reabsorption glomerulosa of
by proximal tubule) adrenal cortex)
Aldosterone
(enhances Na+ reabsorption by collecting tubule)
•So stimulation of RAA system will lead to increase in
plasma volume and edema.

18. 5) INFLAMMATORY EDEMA:-
In acute inflammation—
• vasodilation and • ↑ed vascular permeability
↑ed blood flow through escape of protein-rich
dilated vessels fluid into extravascular tissue
↑hydrostatic pressure in ↓intravascular osmotic
the vessels pressure and ↑osmotic
pressure of the interstitium
marked outflow of fluid and its accumulation in the
interstitial tissue ( EDEMA)

19. Mechanisms involved in oedema by sodium and water retention

20. PATHOGENESIS

21. ACCORDING TO THE DISTRIBUTION ,EDEMA CAN
BE GENERALIZED OR LOCALIZED.
•Localized edema :
causes: a) Venous obstruction : pregnancy,
SVCsyndrome,
IVC syndrome,
varicose veins in
legs, prolonged
recumbency,
venous thrombosis
etc.
b) Lymphatic obstruction: filariasis, Ca breast,
following radical
mastectomy etc.

22. Localized edema contd…..
c)allergic causes : angioneurotic edema,
acute anaphylaxis
d)inflammatory : insect bite, snake
bite,
trauma,ischaemia or
infection
e) miscellaneous : bruises, sprains,
fracture, gout etc.

23. •Generalized edema : it is known as anasarca.
e .g ., Heart diseases like CHF,
pericardial effusion, constrictive
pericarditis.
Cirrhosis of liver,
Nephrotic syndrome,
Malnutrition,
Drugs like nifedipine,
corticosteroids,NSAIDs etc.

24. Depending on the composition of fluid:
transudate & exudate oedema
TRANSUDATE EXUDATE
Definition Filtrate of blood plasma
without changes in
endothelial permeability
Oedema of inflamed
tissue associated with
increased vascular
permeability
Character Non-inflammatory
oedema
Inflammatory oedema
Protein
content
Low (less than 1 gm/dl);
mainly albumin, low
fibrinogen; hence no
tendency to coagulate
High ( 2.5-3.5 gm/dl),
readily coagulates due
to high content of
fibrinogen and other
Coagulation factors
Glucose
content
Same as in plasma Low (less than 60
mg/dl)

25. TRANSUDATE EXUDATE
Specific gravity Low (less than 1.015) High (more than 1.018)
pH > 7.3 < 7.3
LDH Low High
Effusion LDH/ Serum
LDH ratio
< 0.6 > 0.6
Cells Few cells, mainly
mesothelial cells
Many cells, inflammatory
as well as parenchymal
and cellular debris
Examples Oedema in congestive
cardiac failure
Purulent exudate such
as pus

26. SPECIAL FORMS

27. RENAL OEDEMA
• Generalised oedema occurs in certain
diseases of renal origin- such as in
nephrotic syndrome, some types of
glomerulonephritis, and in renal failure
due to acute tubular injury.
• Initially manifests in tissues with loose
connective tissue matrix – eyelids
• Periorbital edema - characteristic

28. Types
• OEDEMA IN NEPHROTIC SYNDROME- Since there is persistent
and heavy proteinuria (albuminuria) in nephrotic syndrome,there is
hypoalbuminaemia causing decreased plasma oncotic pressure
resulting in severe generalised oedema(nephrotic oedema). The
hypoalbuminaemia causes fall in the plasma volume activating
renin-angiotensin-aldosterone mechanism which results in retention
of sodium and water.
• The nephrotic oedema is classically more severe and marked and is
present in the subcutaneous tissues as well as in the visceral
organs. The affected organ is enlarged and heavy with tense
capsule.
• Microscopically, the oedema fluid separates the connective tissue
fibres of subcutaneous tissues. Depending upon the protein content,
the oedema fluid may appear homogeneous, pale, eosinophilic, or
may be deeply eosinophilic and granular.

29. • OEDEMA IN NEPHRITIC SYNDROME- In contrast to nephrotic
oedema, nephritic oedema is not due to hypoproteinaemia but is
largely due to excessive reabsorption of sodium and water in the
renal tubules via renin-angiotensin-aldosterone mechanism. The
protein content of oedema fluid in glomerulonephritis is quite low
(less than 0.5 g/dl).
• The nephritic oedema is usually mild as compared to nephrotic
oedema and begins in the loose tissues such as on the face around
eyes, ankles and genitalia. Oedema in these conditions is usually
not affected by gravity.
• OEDEMA IN ACUTE TUBULAR INJURY- damaged tubules lose
their capacity for selective reabsorption and concentration of the
glomerular filtrate resulting in increased reabsorption.

30. Differences between Nephrotic and Nephritic
Oedema
Feature Nephrotic Nephritic
Cause Nephrotic syndrome Glomerulonephritis
(acute, rapidly
progressive)
Proteinuria Heavy Mild to Moderate
Mechanism ↓Plasma oncotic
Pressure and
Na+ and water
retention
Na+ and water
retention
Degree of oedema Severe, generalised Mild
Distribution Subcutaneous tissues
as well as visceral
organs
Loose tissues mainly
(face, eyes, ankles,
genitalia)

31. PULMONARY OEDEMA
• CAUSES - left ventricular failure, renal
failure, acute respiratory distress
syndrome and pulmonary inflammation or
infection
• CONSEQUENCES - impede oxygen
diffusion- hypoxia – hypercapnia
-favorable environment – bacterial
infection

32. Mechanisms involved in the pathogenesis of pulmonary oedema. A, Normal fluid
exchange at the alveolocapillary membrane (capillary endothelium and alveolar
epithelium). B, Pulmonary oedema via elevated pulmonary hydrostatic pressure. C,
Pulmonary oedema via increased vascular permeability.

33. HAPE
• After an altitude of 2500 metres
• Without halt or waiting for acclimatisation to set
in
• Appearance of oedema fluid -lungs,
congestion – widespread minute haemorrhages
• Gross- the lungs are heavy,moist and
subcrepitant.
• Cut surface exudes frothy fluid (mixture of air
and fluid).

34. • M/E: Interstitial oedema -alveolar oedema
• Congestion –alveolar capillaries
• Alveoli filled with a homogeneous,pink-
staining fluid permeated by air bubbles

35. The alveolar capillaries are congested. The alveolar spaces as well as interstitium
contain eosinophilic, granular, homogeneous and pink proteinaceous oedema fluid
alongwith some RBCs and inflammatory cells.

36. CHF EDEMA
• INCREASED VENOUS PRESSURE
DUE TO FAILURE
• DECREASED RENAL PERFUSION,
triggering of RENIN-
ANGIOTENSION-ALDOSTERONE
complex, resulting ultimately in
SODIUM RETENTION

38. HEPATIC OEDEMA
• i) Hypoproteinaemia - impaired synthesis of proteins
• ii) Portal hypertension - increased venous pressure in
the abdomen - raised hydrostatic pressure.
• iii) Failure of inactivation of aldosterone
-hyperaldosteronism.
• iv) Secondary stimulation of RAAS- sodium and water
retention.

39. CEREBRAL OEDEMA
• Brain edema -localized or generalized - nature extent
-pathologic process or injury. 3 types-
• VASOGENIC OEDEMA : increased filtration pressure or
increased capillary permeability
• CYTOTOXIC OEDEMA : disturbance in the cellular
osmoregulation – response to cell injury
• INTERSTITIAL OEDEMA : hydrocephalus

40. MISCELLANEOUS
• Nutritional Oedema-
• Due to nutritional deficiency of Proteins (Kwashiorkor, prolonged
starvation, famine, fasting), Vitamins (beri-beri due to vitamin B1
deficiency) and Chronic alcoholism
• Main contributing factors- Hypoproteinaemia & Sodium-water
retention
• Myxoedema-
• Hypothyroidism –non pitting oedema occuring on skin of face and
internal organs due to excessive deposition of glycosaminoglycans
in the interstitium
• Microscopically –basophilic mucopolysaccharides.

41. THANK YOU